Effect of switching glatiramer acetate formulation from 20 mg daily to 40 mg three times weekly on immune function in multiple sclerosis.
Multiple sclerosis
cytokines
glatiramer acetate
regulatory T-cells
Journal
Multiple sclerosis journal - experimental, translational and clinical
ISSN: 2055-2173
Titre abrégé: Mult Scler J Exp Transl Clin
Pays: United States
ID NLM: 101668877
Informations de publication
Date de publication:
Historique:
received:
18
04
2021
revised:
22
06
2021
accepted:
24
06
2021
entrez:
11
8
2021
pubmed:
12
8
2021
medline:
12
8
2021
Statut:
epublish
Résumé
Many RRMS patients who had been treated for over 20 years with GA 20 mg/ml daily (GA20) switched to 40 mg/ml three times-a-week (GA40) to reduce injection-related adverse events. Although GA40 is as effective as GA20 in reducing annualized relapse rate and MRI activity, it remains unknown how switching to GA40 from GA20 affects the development of pathogenic and regulatory immune cells. To investigate the difference in immunological parameters in response to GA20 and GA40 treatments. We analyzed five pro-inflammatory cytokines (IL-1β, IL-23, IL-12, IL-18, TNF-α), and three anti-inflammatory/regulatory cytokines (IL-10, IL-13, and IL-27) in serum. In addition, we analyzed six cytokines (IFN-γ, IL-17A, GM-CSF, IL-10, IL-6, and IL-27) in cultured PBMC supernatants. The development of Th1, Th17, Foxp3 Tregs, M1-like, and M2-like macrophages were examined by flow cytometry. Samples were analyzed before and 12 months post switching to GA40 or GA20. Pro- and anti-inflammatory cytokines were comparable between the GA40 and GA20 groups. Development of Th1, Th17, M1-like macrophages, M2-like macrophages, and Foxp3 Tregs was also comparable between the two groups. The immunological parameters measured in RRMS patients treated with GA40 three times weekly are largely comparable to those given daily GA20 treatment.
Sections du résumé
BACKGROUND
BACKGROUND
Many RRMS patients who had been treated for over 20 years with GA 20 mg/ml daily (GA20) switched to 40 mg/ml three times-a-week (GA40) to reduce injection-related adverse events. Although GA40 is as effective as GA20 in reducing annualized relapse rate and MRI activity, it remains unknown how switching to GA40 from GA20 affects the development of pathogenic and regulatory immune cells.
OBJECTIVE
OBJECTIVE
To investigate the difference in immunological parameters in response to GA20 and GA40 treatments.
METHODS
METHODS
We analyzed five pro-inflammatory cytokines (IL-1β, IL-23, IL-12, IL-18, TNF-α), and three anti-inflammatory/regulatory cytokines (IL-10, IL-13, and IL-27) in serum. In addition, we analyzed six cytokines (IFN-γ, IL-17A, GM-CSF, IL-10, IL-6, and IL-27) in cultured PBMC supernatants. The development of Th1, Th17, Foxp3 Tregs, M1-like, and M2-like macrophages were examined by flow cytometry. Samples were analyzed before and 12 months post switching to GA40 or GA20.
RESULTS
RESULTS
Pro- and anti-inflammatory cytokines were comparable between the GA40 and GA20 groups. Development of Th1, Th17, M1-like macrophages, M2-like macrophages, and Foxp3 Tregs was also comparable between the two groups.
CONCLUSIONS
CONCLUSIONS
The immunological parameters measured in RRMS patients treated with GA40 three times weekly are largely comparable to those given daily GA20 treatment.
Identifiants
pubmed: 34377526
doi: 10.1177/20552173211032323
pii: 10.1177_20552173211032323
pmc: PMC8330487
doi:
Types de publication
Journal Article
Langues
eng
Pagination
20552173211032323Informations de copyright
© The Author(s) 2021.
Références
J Immunol. 2003 May 1;170(9):4483-8
pubmed: 12707324
J Immunol. 2008 May 1;180(9):6411-20
pubmed: 18424765
Neurology. 2001 Jul 24;57(2):342-4
pubmed: 11468327
J Neuroimmunol. 2009 Nov 30;216(1-2):113-7
pubmed: 19646767
J Clin Invest. 2000 Apr;105(7):967-76
pubmed: 10749576
J Immunol. 2004 Jun 1;172(11):7144-53
pubmed: 15153538
Ann Neurol. 2013 Jun;73(6):705-13
pubmed: 23686821
Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4355-9
pubmed: 19255448
J Neuroimmunol. 2017 Mar 15;304:21-28
pubmed: 27449853
Neurology. 1998 Mar;50(3):701-8
pubmed: 9521260
Lancet. 2009 Oct 31;374(9700):1503-11
pubmed: 19815268
Neurology. 2000 Dec 12;55(11):1704-14
pubmed: 11113226
Scand J Clin Lab Invest. 2017 Jul;77(4):283-288
pubmed: 28319417
F1000Prime Rep. 2014 Mar 03;6:13
pubmed: 24669294
J Clin Invest. 2005 Jul;115(7):1953-62
pubmed: 16007258
J Neurol Sci. 2018 Apr 15;387:152-156
pubmed: 29571854
N Engl J Med. 1987 Aug 13;317(7):408-14
pubmed: 3302705
J Neuroimmunol. 1998 Dec 1;92(1-2):113-21
pubmed: 9916886
Mult Scler Relat Disord. 2015 Jul;4(4):370-6
pubmed: 26195058
Immunopharmacol Immunotoxicol. 1998 Aug;20(3):373-82
pubmed: 9736442
Clin Exp Immunol. 2003 Sep;133(3):454-60
pubmed: 12930374
Autoimmunity. 2003 May;36(3):133-41
pubmed: 12911279
Cold Spring Harb Perspect Med. 2019 Feb 1;9(2):
pubmed: 29440323
Cells. 2019 Jun 05;8(6):
pubmed: 31195710
Mult Scler. 2017 May;23(6):818-829
pubmed: 27503905
Ann Neurol. 2011 Jan;69(1):75-82
pubmed: 21280077
Neurology. 1995 Jul;45(7):1268-76
pubmed: 7617181
JAMA Neurol. 2014 Nov;71(11):1421-8
pubmed: 25264704
Ann Neurol. 2001 Mar;49(3):290-7
pubmed: 11261502
J Neuroimmunol. 2016 Aug 15;297:1-8
pubmed: 27397070
Pharmacol Ther. 2003 May;98(2):245-55
pubmed: 12725872